Sleep Disordered Breathing in Cardiac Failure
Congestive cardiac failure (CCF) is a widely prevalent and serious problem worldwide with more than 20 million people affected. Despite many recent advances in evaluation and management of heart failure mortality remains high. 40% of patients die within one year of diagnosis and 60 to 70% die within 5 years.1
Sleep disordered breathing occurs frequently in patients with congestive cardiac failure. Predominant types of sleep disordered breathing observed are obstructive sleep apnea (OSA) and central sleep apnea (CSA). Cheyne Stokes respiration (CSR) with central sleep apnea is a type of periodic breathing particularly common in patients with cardiac failure, with waxing and waning pattern of tidal volume.2
Various previous studies have estimated prevalence of sleep disordered breathing (SDB) in congestive cardiac failure to be around 40 to 70%.3â€“6 These figures are higher than the prevalence of SDB in the general population which is estimated to be 19.5% in urban Indian males and of obstructive sleep apnea syndrome at 7.5%.7 Unpublished data from a recently conducted prospective study at Hinduja Hospital, Mumbai showed the prevalence of SDB in stable patients with CCF to be 80%. Obstructive sleep apnea was the commonest pattern observed in 60% of patients and CSA-CSR in 20% of the enrolled patients (fig 1).
Predicting CSR in CCF is not easy as sleepiness, fatigue and disturbed sleep are non specific symptoms which occur in many CCF patients including those without CSR. Sleep quality in patients with Cheyne Stokes respiration is very poor because of constant arousals needed to terminate each apnea. This adds to the great fatigue these patients with CCF feel anyway. Some other clinical features of CSR are that it occurs in non-REM sleep and as the apneas are central, snoring is not common. Desaturation too is seldom as profound as in OSA. Older age, male sex, hypocapnea, elevated LV filling pressure, atrial fibrillation have been identified as potential risk factors for presence of SDB in heart failure.2 However CSA-CSR can occur in symptomatic and also asymptomatic LV systolic dysfunction. Symptom severity, exercise capacity, subjective daytime sleepiness and NT-BNP levels do not increase the likelihood of SDB in CCF.4 In our study there was no significant correlation between LVEF, day time PCO2, serum norepinephrine (marker of sympathetic activity) and apnea-hypopnea index (AHI).
SDB may be a consequence of heart failure as indices of SDB improve with treatment of cardiac failure or it may contribute to the progression of heart failure. Presence of SDB is associated with serious cardiovascular consequences due to repeated episodes of nocturnal desaturations, sympathetic nervous system stimulation, recurrent myocardial hypoxemia and increased oxygen demand. In CCF, presence of SDB is a marker of poor prognosis as these patients are more likely to have hypertension, arrhythmias and worsening of congestive cardiac failure. Presence of CSA-CSR increases the risk of premature death in heart failure. OSAS can also adversely affect heart failure by large intrathoracic pressure swings, increased venous return and consequently increased ventricular afterload.2, 8
Fig. 1. Distribution of SDB in 70 enrolled patients with heart failure at P. D. Hinduja hospital.
The mechanism of CSA-CSR in patients with heart failure is complex and believed to be due to respiratory control system instability secondary to the effects of elevated LV filling pressures, pulmonary congestion, increased peripheral and central chemoreceptor sensitivity and prolonged circulatory time.2
Since the mortality of heart failure is high, any intervention that can affect outcome is worth pursuing vigorously. We would suggest that ideally all patients with CCF should be screened for SDB and CSR by polysomnography (PSG). The good news is that continuous positive airway pressure (CPAP) can impact favorably on CSA in CCF. Patients report great symptomatic improvement in their dyspnea and fatigue, improvements in LVEF are reported and adrenergic drive decreases. Thus CPAP may be as useful an intervention in CCF as any drug therapy including ACE inhibitors.8 The disappointing news is that a large recently concluded study (CANPAP) showed this did not translate into improvement in mortality and survival.10
To conclude CCF and SDB is an area where pulmonologist and cardiologist can closely work together. We need to identify these patients (who are at high risk of death) by performing PSG on them. Then offering them treatment with CPAP can result in symptomatic improvement and actual objective improvement in dyspnea, effort capacity and LV function. Offering our patients with CCF and SDB CPAP therapy should eventually become as routine as treating them with digitalis, diuretics and ACE inhibitors.
D. Agrawal, Clinical Assistant
Z. F. Udwadia, Consultant Chest physician
Respiratory Medicine Department
P. D. Hinduja Hospital, Mumbai
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